Manganese Detoxification by MntE Is Critical for Resistance to Oxidative Stress and Virulence of Staphylococcus aureus Original paper
Researched by:
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Divine Aleru
ID
Divine Aleru
Read MoreI am a biochemist with a deep curiosity for the human microbiome and how it shapes human health, and I enjoy making microbiome science more accessible through research and writing. With 2 years experience in microbiome research, I have curated microbiome studies, analyzed microbial signatures, and now focus on interventions as a Microbiome Signatures and Interventions Research Coordinator.
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Metals
Metals
Heavy metals influence microbial pathogenicity in two ways: they can be toxic to microbes by disrupting cellular functions and inducing oxidative stress, and they can be exploited by pathogens to enhance survival, resist treatment, and evade immunity. Understanding metal–microbe interactions supports better antimicrobial and public health strategies.
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Divine Aleru
Read More
Researched by:
-
Divine Aleru
ID
Divine Aleru
Read More
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Divine Aleru
What was studied?
This study examined the manganese (Mn) detoxification mechanism in Staphylococcus aureus by identifying the role of MntE, a member of the cation diffusion facilitator (CDF) protein family. The research focused on how MntE helps to maintain intracellular Mn homeostasis, which is crucial for resistance to oxidative stress and for the bacterium’s virulence during infection.
Who was studied?
The study primarily focused on Staphylococcus aureus, specifically investigating the role of MntE and MntR, two key proteins involved in regulating Mn homeostasis. The research also used various mutant strains of S. aureus, including MntE and MntR knockouts, to assess the effects of disrupted Mn detoxification.
What were the most important findings?
The study found that MntE is crucial for detoxifying excess Mn in S. aureus, particularly under conditions of Mn overload. MntE-mediated efflux prevents Mn accumulation, which would otherwise lead to toxicity and disrupt cellular function. Mutants lacking MntE showed increased Mn accumulation and decreased resistance to oxidative stress, particularly when exposed to oxidants like sodium hypochlorite (NaOCl) and paraquat. Moreover, the mntE mutants exhibited reduced virulence in a mouse model of systemic infection, as evidenced by significantly lower survival rates compared to wild-type S. aureus strains. MntR, a transcriptional regulator, was found to control the expression of MntE, suggesting that the regulation of Mn homeostasis is tightly coordinated. Additionally, the study highlighted an inverse relationship between intracellular Mn and iron (Fe) levels, implying that excess Mn affects the balance of essential metals in the cell.
What are the greatest implications of this study?
The findings underscore the importance of Mn homeostasis in bacterial pathogenesis and stress the potential of targeting MntE for developing new antimicrobial therapies. Disrupting Mn detoxification could weaken S. aureus, making it more susceptible to host immune defenses, particularly oxidative stress responses. Furthermore, the study provides insights into how S. aureus adapts to fluctuating Mn levels during infection, which could guide future research into managing metal availability as a strategy to control bacterial virulence.
Manganese (Mn)
Manganese plays a pivotal role in microbial pathogenesis. As a vital cofactor for enzymes involved in antioxidant defense and metabolism, manganese is essential for pathogens, enabling them to survive within the host. However, when not properly managed, manganese can become toxic to both the host and the pathogen. The host’s immune system, through mechanisms like the secretion of calprotectin, tries to limit microbial access to manganese, creating an ongoing battle between host defenses and microbial survival .